ABSTRACT
Objective@#To explore the effects of oleic acid and palmitic acid on lipid deposition and mTOR/S6K1/SREBP-1c pathways in HepG2 cells.@*Methods@#The model of steatosis was established with induction of oleic acid and palmitic acid and was intervened by rapamycin. The changes in lipid droplets were observed after staining the cells with oil Red O. Intracellular triglyceride (TG) contents in cells were measured by TG kit. mTOR, S6K1, and SREBP-1c mRNA expression levels were detected using QRT-PCR. Western blot was used to determine protein expression levels of mTOR, S6K1 and SREBP-1c.@*Results@#Both fatty acids increased lipid droplets in HepG2 cells. Fatty degeneration with elevated TG occurred with significant changes in oleic acid group lipids. Rapamycin alleviated lipid deposition caused by oleic acid and palmitic acid and inhibited their induction of increased expression of mTOR, S6K1, and SREBP-1c. QRT-PCR and Western blot results showed that mRNA and protein expressions of mTOR, S6K1, and SREBP-1c in oleic acid and palmitic acid group were significantly higher than the control group (P < 0.05). The increase was more pronounced in the palmitic acid group (P < 0.05); however, after rapamycin intervention, the expression of mRNA and protein in the three groups were significantly lower (P < 0.05), and the change in palmitic acid group was more pronounced (P < 0.05).@*Conclusion@#Oleic acid and palmitic acid can induce lipid deposition in HepG2 cells and increase expression of every component of mTOR/S6K1/SREBP-1c pathway; however, Oleic acid-induced lipid deposition is more pronounced, and the mTOR, S6K1, and SREBP-1c pathway change is more obvious in palmitic acid. Rapamycin has high potent inhibitory effect on palmitic acid-induced lipid deposition. These results specify that lipid synthesis involved in the mTOR/S6K1/SREBP-1c pathways are mainly associated to palmitic acid in HepG2 cells, whereas other signaling pathway may mediate oleic acid-induced lipid synthesis.